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At least 397 records · Page 22Linked to original sources

PubMed1995

Ability of some K+ channel blockers to reverse inhibition of electrically evoked contractions of longitudinal muscle-myenteric plexus.

Blockers selective for different potassium (K+) channels were examined for their ability to reverse inhibition of electrically evoked contractions of longitudinal muscle-myenteric plexus (lm-mp) by adenosine analogs. Cyclohexyl adenosine (CHA) was selected for these studies, since it effectively inhibited contraction (EC50 33 nM). 4-aminopyridine (4-AP) antagonized the inhibition by the adenosine analog, but also stimulated contraction by itself. alpha- and gamma-dendrotoxin produced the most profound reversal of CHA-induced inhibition, while producing a minimal contraction alone. Other blockers produced only nominal reversal of the CHA-induced inhibition. These results suggest that inhibition by CHA is mediated via activation of an alpha- and gamma-dendrotoxin-sensitive K+ channel.

4-Aminopyridine↗

PubMed1978

Methadone detection in rat myenteric plexus: comparison with findings in the central nervous system by the immunofluorescence method.

Nonpregnant and pregnant rats were given methadone for varying time periods. Myenteric plexus was then examined for methadone by immunofluorescence and the results compared to similar studies of the central nervous system. Nonpregnant animals showed positive ganglion cells 2 weeks before methadone was detected in the brain. Additionally, maternal ganglion cells were more frequently positive than those of their offspring. These findings indicate fundamental differences in the response of peripheral and central neurons to methadone. Thus, studying the effects of opiates on isolated strips of bowel may be of little value in furthering understanding of the action of narcotics upon the brain.

Animals↗

PubMed1999

Postnatal development of nitrergic neurons in the myenteric plexus of rat stomach.

The effect of age on the proportion of nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd)-positive neurons was investigated in the myenteric plexus of five different gastric areas of 1-day-, 1-week-, 2-week-, 1-month- and 2-month-old rats. Protein gene product 9.5 immunocytochemistry was used as a marker for the total enteric neuron population in order to establish the percentage of gastric nitrergic neurons in relation to age. The percentage of NADPHd-positive neurons in the proximal parts of the rat stomach (34-38%) is significantly higher than in the antral part (29%). This difference persists in all the age groups investigated. No significant relative increase with age of NADPHd-positive neurons could be observed in any of the areas studied. These findings imply that the increased nitrergic response in the rat proximal stomach as seen in pharmacological studies cannot be explained by an increased relative number of nitrergic neurons.

Animals↗

PubMed2005

Trypanosoma cruzi: preliminary investigation of NADH-positive and somatostatin-immunoreactive neurons in the myenteric plexus of the mouse colon during the infection.

In this paper, the distribution of NADH-positive and somatostatin (SOM) immunoreactive neurons in the myenteric plexus of the colon of mice infected with Trypanosoma cruzi was studied. Ten young, male, BALB/c mice were inoculated with the Y strain of T. cruzi, 60 days previously (chronic phase of the infection). Another 10 mice were uninfected controls. Distal and proximal colonic neurons from five chronically infected mice and their controls were stained using the NADH-diaphorase method. Quantitative results showed a significant decrease of 39% in the number of neurons in the proximal colon of infected mice and 58% in the distal colon (p<0.05). SOM was localized in five animals from each group by light microscopy, using an indirect immunofluorescence technique. It was observed that there were far fewer nerve cells and fibres and less intensely stained neuron bodies and varicose SOM-positive nerve fibres in both, control and chronic infected mice. These findings could be related to the disturbances in intestinal motility observed in patients in the chronic phase of Chagas' disease.

Animals↗

PubMed1984

Electrophysiology and enkephalin immunoreactivity of identified myenteric plexus neurones of guinea-pig small intestine.

Intracellular injection of the fluorescent dye, Lucifer Yellow CH, revealed the shapes of neurones in the myenteric plexus of the guinea-pig ileum, and these shapes were correlated with the electrophysiological properties and enkephalin immunoreactivity of the neurones. A total of eighty-three neurones were filled using electrodes containing a 5% solution of the dye. Forty-six cells had many short processes and a single long process (Dogiel type 1) and twenty-four cells had essentially smooth somas and one to eight long processes (Dogiel type II). Thirteen cells could not be put into either group. Enkephalin-like immunoreactivity was detected in twenty-two of the forty-six Dogiel type I cells. Eighteen of these had club-like short processes. No other cells of the eighty-three showed enkephalin-like immunoreactivity. Electrodes filled with a 0.5% solution of Lucifer Yellow in 0.5 M-KCl were used to record from and simultaneously to inject dye into 240 neurones. Eighty-six nerve cells had a slow after-hyperpolarization following the action potential (AH cells) and forty-six nerve cells had no after-hyperpolarization but exhibited a fast excitatory synaptic potential (S cells). The other cells could not be unequivocally identified by their observed electrophysiological characteristics. Almost all S cells (forty-two of forty-six) were Dogiel type I, while eighty-two of the eighty-six AH cells were Dogiel type II. Fifty S cells (eight located geometrically, forty-two by dye injection) and ninety-one AH cells (twenty-six located geometrically, sixty-five by dye injection) were examined for enkephalin immunoreactivity. Fifteen of the S cells were reactive, whereas all of the AH cells were unreactive. It appears that prolonged impalements reduce immunoreactivity so that the proportion of reactive neurones in this series is an underestimate of the true proportion of S cells with enkephalin-like immunoreactivity. The results suggest that a substantial proportion of the S cells in myenteric ganglia contain enkephalin immunoreactivity while none of the AH cells do. The enkephalin neurones have a distinctive shape and are all Dogiel type I cells. AH cells are nearly always Dogiel type II.

Action Potentials↗

PubMed2004

Presynaptic modulation of cholinergic and non-cholinergic fast synaptic transmission in the myenteric plexus of guinea pig ileum.

Abstract These studies investigated receptors modulating release of mediators of fast excitatory postsynaptic potentials (fEPSPs) in guinea pig ileum myenteric plexus using electrophysiological methods. Fast EPSPs inhibited by >95% by hexamethonium (100 micromol L(-1)) were cholinergic; mixed fEPSPs were inhibited <95% by hexamethonium. Non-cholinergic fEPSPs were studied in the presence of hexamethonium. The alpha2-adrenergic receptor agonist UK 14304 inhibited cholinergic (maximum inhibition = 76%, EC(50) = 18 nmol L(-1)), mixed (81%, 21 nmol L(-1)) and non-cholinergic (76%, 44 nmol L(-1)) fEPSPs equally. The 5-HT(1) receptor agonist 5-carboxamidotryptamine inhibited cholinergic, mixed and non-cholinergic fEPSPs equally. Renzapride, increased non-cholinergic (33%) less than mixed (97%, 13 micromol L(-1)) fEPSPs. Renzapride inhibited the purely cholinergic fEPSPs (-29%) but potentiated the cholinergic component of mixed fEPSPs (39%). Prucalopride potentiated all fEPSPs equally (30-33%). 5-HT (0.1 micromol L(-1)) induced potentiation of cholinergic (75%), mixed (97%) and non-cholinergic (84%) fEPSPs was not statistically different. The potentiating effects of renzapride and 5-HT on fEPSPs were inhibited by the 5-HT(4) receptor antagonist, SB 204070 (10 nmol L(-1)). Renzapride (0.3 micromol L(-1)) blocked 5-HT-induced increases in cholinergic fEPSPs. alpha2-Adrenergic and 5-HT(1) receptors mediate inhibition of transmitter release from cholinergic and mixed terminals. 5-HT and prucalopride, acting at 5-HT(4) receptors, facilitate all fEPSPs; renzapride facilitates the cholinergic and non-cholinergic components of mixed fEPSPs but not purely cholinergic fEPSPs. Cholinergic synapses may express few 5-HT(4) receptors or a renzapride-insensitive 5-HT(4) receptor isoform.

Acetylcholine↗

PubMed1982

Possible modulatory role of dynorphin on the excitation by neurotensin on the guinea pig myenteric plexus.

Dynorphin 1-13 antagonized in a concentration-dependent fashion the contractile effect of neurotensin on the isolated preparation of the guinea pig ileum myenteric plexus. The inhibitory action of dynorphin was reduced in the presence of naloxone indicating the opioid nature of this interaction. Atropine also reduced the excitatory component of the neurotensin-induced contractile response; the joint application of atropine plus dynorphin did not cause additional inhibition of the contractile effect of neurotensin.

Animals↗

PubMedDate not supplied

Morphological and quantitative study of the myenteric plexus of the duodenum of streptozotocin-induced diabetic rats.

The purpose of this work was to study the morphological and quantitative alterations of the myenteric plexus neurons of the duodenum of rats with acute and chronic streptozotocin-induced diabetes and establish a comparison with non-diabetic animals. Samples of duodenum were destined to histological sections stained by Hematoxilin-Eosin and to membrane preparings stained by the Giemsa and NADH-diaphorasis methods. Small, medium and large neurons were found, with a predominance of medium ones on chronic and acute diabetic animals. It was verified that most of the neurons of diabetic and non-diabetic animals have an eccentrical nucleus and thus this characteristic is not an indicative of degenerative process. It was observed that in diabetes there is a decrease in the number of myenteric neurons. It is argued that this initial decrease is due to the toxic effects of the drug and not to the physiopathology of diabetes itself, and also that the expressive smaller proportion of neurons on the chronically diabetic animals is due to the immediate loss related to streptozotocin and the further consequences of aging during nine weeks of diabetes.

Animals↗

PubMed1986

Effect of external Ca2+ on the spontaneous and the various stimuli-induced acetylcholine release from guinea-pig ileum myenteric plexus.

Effect of external Ca2+ concentration ([Ca2+]o) on spontaneous and various types of stimuli-induced acetylcholine (ACh) release from guinea-pig ileum myenteric plexus was studied. Electrical field stimulation- or high-K+-induced ACh release increased with the increment of [Ca2+]o. On the other hand, the spontaneous and the nicotine-induced ACh release increased up to 0.45 mM [Ca2+]o and then declined progressively as [Ca2+]o was raised. Qualitatively similar results were obtained with dimethylphenylpirerazinium-, 5-hydroxytryptamine- and substance P-induced ACh release. These results were discussed in terms of the stabilizing effect of Ca2+.

Acetylcholine↗

PubMed1989

Electrical and synaptic properties of myenteric plexus neurones in the terminal large intestine of the guinea-pig.

1. Intracellular recording methods were used to investigate the cellular neurophysiology of ganglion cells in the myenteric plexus of the guinea-pig rectum. The rectum is a region of the gastrointestinal tract with specialized functions that include reflex relaxation of the internal and sphincter during defaecation. Electrical and synaptic properties of myenteric neurones in the rectum had not previously been studied. Therefore, the overall aim of the work was to describe electrical and synaptic behaviour and identify neurophysiological properties of rectal neurones that might be related to specialization of function in this region of the gut. 2. Thirty-four (58%) of fifty-nine impaled cells had electrophysiological properties of AH/type 2 enteric neurones. Eighteen (30%) behaved like type 3 neurones and only two (3%) behaved like S/type 1 enteric neurones. Three per cent were presumably glial cells and the remainder were unclassifiable. 3. Nicotinic cholinergic fast EPSPs were recorded in six of thirty-four (18%) of AH/type 2 neurones and in all eighteen of the type 3 cells. Slow EPSPs occurred in five of thirty-four (15%) of AH/type 2 neurones and were absent from type 3 neurones. 4. Type 3 neurones received fast synaptic inputs from axons in each of the interganglionic fibre tracts that were connected with the ganglion containing the neurone. 5. AH/type 2 neurones were apparently multipolar neurones with long processes projecting into each of the interganglionic fibre tracts connected with the ganglion. Type 3 neurones did not have processes leaving the ganglion in the fibre tracts. 6. Run-down in amplitude of the fast EPSPs in type 3 neurones occurred when they were evoked at frequencies of 5 Hz or greater. 7. Presynaptic muscarinic cholinergic receptors behaved like autoreceptors in suppressing the release of acetylcholine at nicotinic synapses on type 3 neurones. 8. Application of 5-hydroxytryptamine, acetylcholine, substance P and forskolin mimicked the characteristics of slow EPSPs in the AH/type 2 neurones. 9. The principal difference between neuronal behaviour in the rectum and small intestine, colon and stomach was in the relative proportions of AH/type 2, S/type 1 and type 3 neurones. This is discussed in terms of the functional specialization of the rectum.

Acetylcholine↗

PubMed1989

The development and reversal of the tolerance to morphine in the longitudinal smooth muscle-myenteric plexus preparation of the guinea pig.

Chronic treatment with morphine results in a reduction in the potency of morphine in the longitudinal smooth muscle-myenteric plexus of the guinea-pig ileum. Implantation of morphine pellets leads to the development of tolerance to the inhibitory effects of morphine upon neurogenic contractions of this preparation. Tolerance develops within 24 hours, peaks between days 4 and 7 and disappears by day 14. A similar time course for the development of tolerance to the inhibitory effects of 2-chloroadenosine is also seen in these same morphine-tolerant preparations. The rate of reversal of morphine tolerance was assessed after the removal of the morphine pellets four days after implantation. In this situation, tolerance to the effects of morphine were maintained for at least 24 hours, were partially reversed at day 2 and were totally reversed by day 4. The delay in the development and reversal of the effect are consistent with the fact that chronic treatment with morphine evokes an adaptive sensitivity change.

2-Chloroadenosine↗

PubMed2000

Ryanodine-sensitive stores regulate the excitability of AH neurons in the myenteric plexus of guinea-pig ileum.

Myenteric afterhyperpolarizing (AH) neurons are primary afferent neurons within the gastrointestinal tract. Stimulation of the intestinal mucosa evokes action potentials (AP) that are followed by a slow afterhyperpolarization (AHP(slow)) in the soma. The role of intracellular Ca(2+) ([Ca(2+)](i)) and ryanodine-sensitive Ca(2+) stores in modulating the electrical activity of myenteric AH neurons was investigated by recording membrane potential and bis-fura-2 fluorescence from 34 AH neurons. Mean resting [Ca(2+)](i) was approximately 200 nM. Depolarizing current pulses that elicited APs evoked AHP(slow) and an increase in [Ca(2+)](i), with similar time courses. The amplitudes and durations of AHP(slow) and the Ca(2+) transient were proportional to the number of evoked APs, with each AP increasing [Ca(2+)](i) by approximately 50 nM. Ryanodine (10 microM) significantly reduced both the amplitude and duration (by 60%) of the evoked Ca(2+) transient and AHP(slow) over the range of APs tested (1-15). Calcium-induced calcium release (CICR) was graded and proportional to the number of APs, with each AP triggering a rise in [Ca(2+)](i) of approximately 30 nM Ca(2+) via CICR. This indicates that CICR amplifies Ca(2+) influx. Similar changes in [Ca(2+)](i) and AHP(slow) were evoked by two APs in control and six APs in ryanodine. Thus, the magnitude of the change in bulk [Ca(2+)](i) and not the source of the Ca(2+) is the determinant of the magnitude of AHP(slow). Furthermore, lowering of free [Ca(2+)](i), either by reducing extracellular Ca(2+) or injecting high concentrations of Ca(2+) buffer, induced depolarization, increased excitability, and abolition of AHP(slow). In addition, activation of synaptic input to AH neurons elicited a slow excitatory postsynaptic potential (sEPSP) that was completely blocked in ryanodine. These results demonstrate the importance of [Ca(2+)](i) and CICR in sensory processing in AH neurons. Activity-dependent CICR may be a mechanism to grade the output of AH neurons according to the intensity of sensory input.

Action Potentials↗

PubMed1985

Adrenergic and possible nonadrenergic sources of adenosine 5'-triphosphate release from nerve varicosities isolated from ileal myenteric plexus.

Pretreatment of guinea pigs with 6-hydroxydopamine in vivo for 24 h (250 mg/kg i.p.) reduced the norepinephrine and tyrosine hydroxylase contents of varicosities isolated from ileal myenteric plexus by 91 and 89%, respectively, indicating extensive destruction of noradrenergic varicosities. Destruction appeared to be restricted to noradrenergic varicosities because 5-hydroxytryptamine contents were unaffected. In vivo 6-hydroxydopamine treatment reduced the K+- and veratridine-evoked release of ATP from myenteric varicosities by 56 and 63%, respectively, indicating that much, but not all, of the evoked release of ATP probably originated from noradrenergic varicosities. Pretreatment of guinea pigs with 5 mg/kg of reserpine i.p. depleted norepinephrine contents of isolated varicosities by 90% but did not significantly reduce K+- or veratridine-evoked release of ATP, suggesting that the exocytotic release process was unaffected by reserpine. Selective destruction of serotonergic varicosities by treatment of guinea pigs with 50 mg/kg of desmethylimipramine i.p. followed by 40 mg/kg of 5,7-dihydroxytryptamine s.c. failed to diminish K+- or veratridine-evoked release of ATP from myenteric varicosities, indicating that the nonadrenergic release of ATP did not arise from serotonergic varicosities.

Adenosine Triphosphate↗

PubMed1994

Mechanism underlying tumor necrosis factor-alpha suppression of norepinephrine release from rat myenteric plexus.

We studied the effect of tumor necrosis factor-alpha (TNF-alpha) on the release of [3H]norepinephrine ([3H]NE) from longitudinal muscle-myenteric plexus preparations of rat jejunum. TNF-alpha had no immediate effect on [3H]NE release. Preincubation of the tissue with TNF-alpha caused a suppression of [3H]NE release stimulated by KCl or electrical field stimulation. The action of TNF-alpha was time and concentration dependent (0.1-50 ng/ml) and was not due to endotoxin contamination. The effect of TNF-alpha was biphasic, occurring after 30 min and again after 120 min of preincubation. The early component was independent of protein synthesis but was inhibited by piroxicam or indomethacin, indicating the involvement of cyclooxygenase metabolites. The late component was dependent on protein synthesis, was blocked by an interleukin-1 receptor antagonist, and was inhibited by piroxicam or indomethacin. These results indicate that TNF-alpha suppresses NE release by two mechanisms, one of which is due to the synthesis and release of interleukin-1, each involving arachidonic acid metabolites.

Animals↗

PubMed1994

Muscarinic M1 and M3 receptor antagonist effects of a new pirenzepine analogue in isolated guinea-pig ileal longitudinal muscle-myenteric plexus.

The new pirenzepine analogue DF 545 has been tested for its muscarinic M1 and M3 receptor antagonist properties in guinea-pig longitudinal muscle-myenteric plexus preparations. McN-A-343-induced inhibition of twitch contractions was taken as a parameter for muscarinic M1 receptor activation while electrical and acetylcholine-induced contractions were considered as a model for muscarinic M3 receptor stimulation. An unexpected contractile effect evoked by McN-A-343 was also investigated. In contrast to pirenzepine, DF 545 only weakly counteracted the M1-mediated McN-A-343 inhibitory effect but blocked M3-related twitch- or acetylcholine-stimulated responses with a 2-fold higher affinity than pirenzepine. Therefore, in this preparation, our findings suggest that DF 545 does not share the selectivity profile exhibited by pirenzepine at ileal muscarinic receptors. Studies on the McN-A-343 contractile effect provide evidence that this agonist may interact with ileal muscarinic effector sites in a different way from other cholinergic agents.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗

PubMed1998

Enkephalin-immunoreactive subpopulations in the myenteric plexus of the guinea-pig fundus project primarily to the muscle and not to the mucosa.

Enkephalin (ENK) immunoreactivity was localised in different neuronal subpopulations of the myenteric plexus in the guinea-pig gastric fundus using immunohistochemistry for neurone-specific enolase (NSE), ENK, choline acetyltransferase (ChAT), substance P (SP), neuropeptide Y (NPY), calretinin (CALRET), and somatostatin (SOM). NADPH-diaphorase staining was used to label nitric oxide synthase (NOS)-containing neurones. ENK was observed in 44% of the myenteric neurones. The major ENK-positive subpopulations were ChAT/ENK (35% of ENK-positive neurones), ChAT/SP/ENK (26%), NOS/NPY/ENK (22%) and ChAT/SP/ENK/CALRET (9%). The projection pathways of these ENK-positive subpopulations to the circular muscle and the mucosa were determined using retrograde labelling with DiI in organ culture followed by immunohistochemistry. Of myenteric neurones retrogradely labelled from the mucosa and the circular muscle, 13% and 48% exhibited ENK immunoreactivity, respectively. Three major ENK-positive subpopulations innervating the mucosa or circular muscle were identified: ascending ChAT/SP/ENK (7% of all mucosa neurones; 24% of all circular muscle neurones), ascending ChAT/ENK (4%; 15%) and descending NOS/NPY/ENK (1%; 8%) neurones. Only very few CALRET- or SOM-positive neurones projected to the mucosa or circular muscle. ChAT/SP/ENK and ChAT/ENK neurones might function as ascending excitatory muscle motor neurones, whereas NOS/NPY/ENK neurones are most likely descending inhibitory muscle motor neurones. The relatively few ENK-positive mucosa neurones do not favour a major involvement of ENK-positive myenteric neurones in the control of gastric mucosa activity.

Animals↗

PubMed1992

Effects of 5-HT4 receptor stimulation on basal and electrically evoked release of acetylcholine from guinea-pig myenteric plexus.

The effects of 5-methoxytryptamine and 5-hydroxytryptamine (5-HT) on both basal and electrically evoked outflow of tritium were studied in guinea-pig myenteric plexus preparations preincubated with [3H]-choline. Basal outflow. 5-Methoxytryptamine caused a transient and calcium-dependent increase in basal outflow of [3H]acetylcholine that was abolished by tetrodotoxin. Ondansetron (1 mumol/l) did not affect the stimulatory response of 5-methoxytryptamine but ICS 205-930 (1 and 3 mumol/l) produced parallel rightward displacements of the concentration-response curve to 5-methoxytryptamine. The pKB value for ICS 205-930 was 6.6 suggesting an involvement of 5-HT4 receptors. 5-HT caused an increase in basal outflow of [3H]acetylcholine and a biphasic concentration-response curve was obtained. The maximal response of the first phase to 5-HT (release of 0.98% of tissue tritium) and the maximal response to 5-methoxytryptamine (0.94% of tissue tritium) were similar but 5-methoxytryptamine (-log EC50: 6.9) was less potent than 5-HT (-log EC50 of the high affinity component: 7.9). ICS 205-930 (0.01-1.0 mumol/l) acted as a competitive antagonist against the low affinity component of the 5-HT concentration-response curve with a pA2 value of 8.0. It is concluded that stimulation of both 5-HT4 receptors (by 5-methoxytryptamine and submicromolar concentrations of 5-HT) and 5-HT3 receptors (by micromolar concentrations of 5-HT) causes a release of acetylcholine which in turn leads to smooth muscle contraction. Electrically evoked outflow. This outflow of [3H]-acetylcholine was concentration-dependently inhibited by both 5-methoxytryptamine and 5-HT.(ABSTRACT TRUNCATED AT 250 WORDS)

5-Methoxytryptamine↗

PubMed1996

Chemical coding of neurons in the myenteric plexus and external muscle of the small and large intestine of the mouse.

Immunohistochemical techniques were used to examine the presence and co-localisation of a range of putative neurotransmitters and other neuronal markers in the myenteric plexus of the small and large intestine of the mouse. Distinct sub-populations of myenteric neurons were identified, based on the combinations of substances they contained and the distribution of their fibres. In the small intestine, there were two major classes of circular muscle motor neurons; one class was characterised by the presence of nitric oxide synthase, vasoactive intestinal peptide plus neuropeptide Y (NOS/VIP/NPY), and the second class contained calretinin plus substance P (CalR/SP). There were seven classes of neurons that innervated myenteric ganglia; these contained nos, vip, nos/vip, npy, calr/calbindin (calb), sp or 5-ht. In the large intestine, there were five major classes of motor neurons that contained nos, nos/vip, gaba, sp, or calr/sp, and seven major classes of neurons that innervated myenteric ganglia and contained nos, vip, calr/calb, calr, sp, gaba or 5-ht. Although some aspects of the patterns of co-localisation are similar to those in other species, this study re-inforces recent analyses that indicate significant species differences in neurochemical patterns in the enteric neurons of different species.

Animals↗